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Article ; Online: Corneal Endothelium Viability Assay Using Trypan Blue Dye After Preloaded DMEK Graft Preparation.

Szkarlat, Michael R / Hicks, Nicholas / Titus, Michael S / Sawant, Onkar B

2024

Abstract: Purpose: The purpose of this study was to establish a validated method, consistent with Eye Bank Association of America medical standards, for evaluating endothelial cell loss (ECL) from an entire Descemet membrane endothelial keratoplasty (DMEK) graft ... ...

Abstract	Purpose: The purpose of this study was to establish a validated method, consistent with Eye Bank Association of America medical standards, for evaluating endothelial cell loss (ECL) from an entire Descemet membrane endothelial keratoplasty (DMEK) graft using trypan blue dye as an alternative to specular microscopy. Method: Twenty-nine corneas were prepared for preloaded DMEK by a single technician, and the endothelium was stained with trypan blue dye for 30 seconds. The technician estimated total cell loss as a percentage of the graft and captured an image. Images were evaluated by a blinded technician using ImageJ software to determine ECL and compared with endothelial cell density from specular microscopy. Tissue processing intervals were analyzed for 4 months before and after implementation of this method. Results: For the 29 grafts, there was no statistically significant difference (t test, P = 0.285) between ECL estimated by a processor (mean = 5.8%) and ECL calculated using an ImageJ software (mean = 5.1%). The processor tended to estimate greater ECL than the actual ECL determined by ImageJ (paired t test, P = 0.022). Comparatively, postprocessing endothelial cell density measured by specular microscopy were higher compared with the preprocessing endothelial cell density (mean = 4.5% P = 0.0006). After implementation of this evaluation method, DMEK graft processing time intervals were reduced by 47.9% compared with specular microscopy evaluation (P < 0.001). Conclusions: Our results show that visual ECL estimation using trypan blue staining by a DMEK graft processor is a reliable and efficient method for endothelial assessment. Unlike specular microscopy, this method achieves comprehensive visualization of the entire endothelium, reduces total time out of cold storage, and decreases total time required to prepare and evaluate DMEK grafts.
Language	English
Publishing date	2024-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	604826-2
ISSN	1536-4798 ; 0277-3740
ISSN (online)	1536-4798
ISSN	0277-3740
DOI	10.1097/ICO.0000000000003514
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Article ; Online: Povidone-Iodine Attenuates Viral Replication in Ocular Cells: Implications for Ocular Transmission of RNA Viruses.

Singh, Sneha / Sawant, Onkar B / Mian, Shahzad I / Kumar, Ashok

Biomolecules

2021 Volume 11, Issue 5

Abstract: Several RNA viruses, including SARS-CoV-2, can infect or use the eye as an entry portal to cause ocular or systemic diseases. Povidone-Iodine (PVP-I) is routinely used during ocular surgeries and eye banking as a cost-effective disinfectant due to its ... ...

Abstract	Several RNA viruses, including SARS-CoV-2, can infect or use the eye as an entry portal to cause ocular or systemic diseases. Povidone-Iodine (PVP-I) is routinely used during ocular surgeries and eye banking as a cost-effective disinfectant due to its broad-spectrum antimicrobial activity, including against viruses. However, whether PVP-I can exert antiviral activities in virus-infected cells remains elusive. In this study, using Zika (ZIKV) and Chikungunya (CHIKV) virus infection of human corneal and retinal pigment epithelial cells, we report antiviral mechanisms of PVP-I. Our data showed that PVP-I, even at the lowest concentration (0.01%), drastically reduced viral replication in corneal and retinal cells without causing cellular toxicity. Antiviral effects of PVP-I against ZIKV and CHIKV were mediated by direct viral inactivation, thus attenuating the ability of the virus to infect host cells. Moreover, one-minute PVP-I exposure of infected ocular cells drastically reduced viral replication and the production of infectious progeny virions. Furthermore, viral-induced (CHIKV) expression of inflammatory genes (
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Cell Line ; Chikungunya virus/physiology ; Chlorocebus aethiops ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Povidone-Iodine/pharmacology ; RNA Viruses/physiology ; Retinal Pigment Epithelium/cytology ; Retinal Pigment Epithelium/metabolism ; Retinal Pigment Epithelium/virology ; SARS-CoV-2/physiology ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Vero Cells ; Virus Replication/drug effects ; Zika Virus/physiology
Chemical Substances	Antiviral Agents ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Povidone-Iodine (85H0HZU99M)
Language	English
Publishing date	2021-05-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11050753
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Article ; Online: Development of Anterior Segment Focused Biologic Therapies to Regenerate Corneal Tissue for the Treatment of Disease: Drug Development Experience.

Rowe-Rendleman, Cheryl / Eveleth, David / Goldberg, Jeffrey L / Jurkunas, Ula / Okumura, Naoki / Dawson, Daniel / Sawant, Onkar B

Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics

2023 Volume 39, Issue 8, Page(s) 551–562

Abstract: On February 24-27, 2021, the Association for Ocular Pharmacology and Therapeutics (AOPT) held its 15th biennial scientific meeting online. The meeting was organized by Dr. Sanjoy Bhattacharya of the University of Miami in conjunction with the board of ... ...

Abstract	On February 24-27, 2021, the Association for Ocular Pharmacology and Therapeutics (AOPT) held its 15th biennial scientific meeting online. The meeting was organized by Dr. Sanjoy Bhattacharya of the University of Miami in conjunction with the board of trustees of the AOPT. The 3-day conference was attended by academic scientists, clinicians, and industry and regulatory professionals. The theme of the meeting was Restoring Vision through Regeneration and it was sponsored, in part, by the National Institutes of Health, Bright Focus, Regeneron, and Santen (USA). During the 3 days of the meeting, presentations from several sessions explored different aspects of regenerative medicine in ophthalmology, including optic nerve regeneration, drugs and devices in glaucoma, retinal neuroprotection and plasticity, visual perception, and degeneration of trabecular meshwork. This article summarizes the proceedings of the session on corneal regenerative medicine research and discusses emerging concepts in drug development for corneal epithelial and endothelial regeneration. Since the meeting in 2021, several of these concepts have advanced to clinical-stage therapies, but so far as of 2023, none has been approved by regional regulatory authorities in the United States. One form of corneal endothelial cell therapy has been approved in Japan and only for bullous keratopathy. Ongoing work is proceeding in the United States and other countries. Clinical Registration No: National Clinical Trials 04894110, 04812667; Japan Registry for Clinical Trials a031210199.
MeSH term(s)	Cornea ; Regenerative Medicine ; Retina ; Biological Therapy ; Drug Development
Language	English
Publishing date	2023-09-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1237021-6
ISSN	1557-7732 ; 1080-7683
ISSN (online)	1557-7732
ISSN	1080-7683
DOI	10.1089/jop.2023.0044
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Article ; Online: Histological characterization of retinal degeneration in mucopolysaccharidosis type IIIC.

Ludwig, Jessica / Sawant, Onkar B / Wood, Jill / Singamsetty, Srikanth / Pan, Xuefang / Bonilha, Vera L / Rao, Sujata / Pshezhetsky, Alexey V

Experimental eye research

2023 Volume 229, Page(s) 109433

Abstract: Heparan-α-glucosaminide N-acetyltransferase (HGSNAT) participates in lysosomal degradation of heparan sulfate. Mutations in the gene encoding this enzyme cause mucopolysaccharidosis IIIC (MPS IIIC) or Sanfilippo syndrome type C. MPS IIIC patients exhibit ...

Abstract	Heparan-α-glucosaminide N-acetyltransferase (HGSNAT) participates in lysosomal degradation of heparan sulfate. Mutations in the gene encoding this enzyme cause mucopolysaccharidosis IIIC (MPS IIIC) or Sanfilippo syndrome type C. MPS IIIC patients exhibit progressive neurodegeneration, leading to dementia and death in early adulthood. Currently there is no approved treatment for MPS IIIC. Incidences of non-syndromic retinitis pigmentosa and early signs of night blindness are reported in some MPS IIIC patients, however the majority of ocular phenotypes are not well characterized. The goal of this study was to investigate retinal degeneration phenotype in the Hgsnat knockout mouse model of MPS IIIC and a cadaveric human MPS IIIC eye. Cone and rod photoreceptors in the eyes of homozygous 6-month-old Hgsnat knockout mice and their wild-type counterparts were analyzed using cone arrestin, S-opsin, M-opsin and rhodopsin antibodies. Histological observation was performed on the eye from a 35-year-old MPS IIIC donor. We observed a nearly 50% reduction in the rod photoreceptors density in the Hgsnat knockout mice compared to the littermate wild-type controls. Cone photoreceptor density was unaltered at this age. Severe retinal degeneration was also observed in the MPS IIIC donor eye. To our knowledge, this is the first report characterizing ocular phenotypes arising from deleterious variants in the Hgsnat gene associated with MPS IIIC clinical phenotype. Our findings indicate retinal manifestations may be present even before behavioral manifestations. Thus, we speculate that ophthalmological evaluations could be used as diagnostic indicators of early disease, progression, and end-point evaluation for future MPS IIIC therapies.
MeSH term(s)	Animals ; Mice ; Humans ; Adult ; Infant ; Mucopolysaccharidosis III/genetics ; Mucopolysaccharidosis III/diagnosis ; Mucopolysaccharidosis III/pathology ; Retinal Degeneration/genetics ; Mutation ; Retinitis Pigmentosa ; Mice, Knockout ; Acetyltransferases/genetics
Chemical Substances	HGSNAT protein, human (EC 2.3.1.78) ; Acetyltransferases (EC 2.3.1.-)
Language	English
Publishing date	2023-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2023.109433
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Article ; Online: Neuronal Bmal1 regulates retinal angiogenesis and neovascularization in mice

Vijay K. Jidigam / Onkar B. Sawant / Rebecca D. Fuller / Kenya Wilcots / Rupesh Singh / Richard A. Lang / Sujata Rao

Communications Biology, Vol 5, Iss 1, Pp 1-

2022 Volume 11

Abstract: Silencing of the retinal clock through targeting neuronal Bmal1 could constitute an approach to treating some forms of retinopathy. ...

Abstract	Silencing of the retinal clock through targeting neuronal Bmal1 could constitute an approach to treating some forms of retinopathy.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Prenatal alcohol exposure and maternal glutamine supplementation alter the mTOR signaling pathway in ovine fetal cerebellum and skeletal muscle.

Sawant, Onkar B / Meng, Cong / Wu, Guoyao / Washburn, Shannon E

Alcohol (Fayetteville, N.Y.)

2020 Volume 89, Page(s) 93–102

Abstract: Prenatal alcohol exposure causes fetal neurodevelopmental damage and growth restriction. Among regions of the brain, the cerebellum is the most vulnerable to developmental alcohol exposure. Despite vast research in the field, there is still a need to ... ...

Abstract	Prenatal alcohol exposure causes fetal neurodevelopmental damage and growth restriction. Among regions of the brain, the cerebellum is the most vulnerable to developmental alcohol exposure. Despite vast research in the field, there is still a need to identify specific mechanisms by which alcohol causes this damage in order to design effective therapeutic interventions. The mammalian target of rapamycin (mTOR) is known to be associated with axonal regeneration, dendritic arborization, synaptic plasticity, cellular growth, autophagy, and many other cellular processes. Glutamine and glutamine-related amino acids play a key role in fetal development and are known to alter the mTOR pathway; recent research has shown that disturbances in their bioavailability and signaling pathways may mediate adverse effects of prenatal alcohol exposure. This study investigated the role of the mTOR signaling pathway in the fetal cerebellum and skeletal muscle after third trimester-equivalent prenatal alcohol exposure and maternal l-glutamine (GLN) supplementation using a sheep model. Fetal cerebella and skeletal muscles were sampled for Western blot analysis of mTOR and its downstream targets S6 kinase and eukaryotic initiation factor 4E-bindin protein (4E-BP1). The expression of cerebellar phosphorylated mTOR relative to the total mTOR was elevated in the alcohol+GLN group compared to the saline and GLN groups. Alcohol exposure increased the ratio of phosphorylated S6K to total S6K in fetal cerebellum, and no significant effect of GLN supplementation was observed. On contrary, maternal GLN supplementation reduced the activation of mTOR and S6K in fetal skeletal muscle, possibly to make GLN and other amino acids available for use by other organs. These findings suggest prenatal alcohol exposure and maternal GLN supplementation during the third trimester-equivalent alter the mTOR signaling cascade, which plays a possible key role in alcohol-induced developmental damage.
MeSH term(s)	Animals ; Cerebellum/drug effects ; Cerebellum/metabolism ; Dietary Supplements ; Ethanol/adverse effects ; Female ; Glutamine/administration & dosage ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Phosphorylation ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; Sheep ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Glutamine (0RH81L854J) ; Ethanol (3K9958V90M) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Ribosomal Protein S6 Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	605912-0
ISSN	1873-6823 ; 0741-8329
ISSN (online)	1873-6823
ISSN	0741-8329
DOI	10.1016/j.alcohol.2020.08.002
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Article ; Online: Aster proteins mediate carotenoid transport in mammalian cells.

Bandara, Sepalika / Ramkumar, Srinivasagan / Imanishi, Sanae / Thomas, Linda D / Sawant, Onkar B / Imanishi, Yoshikazu / von Lintig, Johannes

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 15, Page(s) e2200068119

Abstract: ... retinas. We previously identified the scavenger receptor class B type 1 and the enzyme β-carotene ... concentrated carotenoids in Aster-B protein-expressing tissues such as the adrenal glands. Remarkably, Aster-B ... was expressed in the human but not in the mouse retina. Within the retina, Aster-B and BCO2 showed ...

Abstract	Some mammalian tissues uniquely concentrate carotenoids, but the underlying biochemical mechanism for this accumulation has not been fully elucidated. For instance, the central retina of the primate eyes displays high levels of the carotenoids, lutein, and zeaxanthin, whereas the pigments are largely absent in rodent retinas. We previously identified the scavenger receptor class B type 1 and the enzyme β-carotene-oxygenase-2 (BCO2) as key components that determine carotenoid concentration in tissues. We now provide evidence that Aster (GRAM-domain-containing) proteins, recently recognized for their role in nonvesicular cholesterol transport, engage in carotenoid metabolism. Our analyses revealed that the StART-like lipid binding domain of Aster proteins can accommodate the bulky pigments and bind them with high affinity. We further showed that carotenoids and cholesterol compete for the same binding site. We established a bacterial test system to demonstrate that the StART-like domains of mouse and human Aster proteins can extract carotenoids from biological membranes. Mice deficient for the carotenoid catabolizing enzyme BCO2 concentrated carotenoids in Aster-B protein-expressing tissues such as the adrenal glands. Remarkably, Aster-B was expressed in the human but not in the mouse retina. Within the retina, Aster-B and BCO2 showed opposite expression patterns in central versus peripheral parts. Together, our study unravels the biochemical basis for intracellular carotenoid transport and implicates Aster-B in the pathway for macula pigment concentration in the human retina.
MeSH term(s)	Animals ; Biological Transport ; Carotenoids/metabolism ; Dioxygenases/genetics ; Dioxygenases/metabolism ; Humans ; Macula Lutea/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice
Chemical Substances	GRAMD1B protein, human ; Membrane Proteins ; Carotenoids (36-88-4) ; Dioxygenases (EC 1.13.11.-) ; Bco2 protein, mouse (EC 1.14.99.-)
Language	English
Publishing date	2022-04-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2200068119
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Article ; Online: Thyroid Activating Enzyme, Deiodinase II Is Required for Photoreceptor Function in the Mouse Model of Retinopathy of Prematurity.

Sawant, Onkar B / Jidigam, Vijay K / Wilcots, Kenya / Fuller, Rebecca D / Samuels, Ivy / Rao, Sujata

Investigative ophthalmology & visual science

2021 Volume 61, Issue 13, Page(s) 36

Abstract: Purpose: Retinopathy of prematurity (ROP) is a severe complication of premature infants, leading to vision loss when untreated. Presently, the molecular mechanisms underlying ROP are still far from being clearly understood. This study sought to ... ...

Abstract	Purpose: Retinopathy of prematurity (ROP) is a severe complication of premature infants, leading to vision loss when untreated. Presently, the molecular mechanisms underlying ROP are still far from being clearly understood. This study sought to investigate whether thyroid hormone (TH) signaling contributes to the neuropathology of ROP using the mouse model of ROP to evaluate longitudinal photoreceptor function. Methods: Animals were exposed to hyperoxia from P7 to P12 to induce retinopathy, thereafter the animals were returned to room air (normoxia). The thyroid-activating enzyme type 2 deiodinases (Dio2) knockout (KO) mice and the littermate controls that were exposed to hyperoxia or maintained in room air and were then analyzed. The retinal function was evaluated using electroretinograms (ERGs) at three and seven weeks followed by histologic assessments with neuronal markers to detect cellular changes in the retina. Rhodopsin protein levels were measured to validate the results obtained from the immunofluorescence analyses. Results: In the ROP group, the photoreceptor ERG responses are considerably lower both in the control and the Dio2 KO animals at P23 compared to the non-ROP group. In agreement with the ERG responses, loss of Dio2 results in mislocalized cone nuclei, and abnormal rod bipolar cell dendrites extending into the outer nuclear layer. The retinal function is compromised in the adult Dio2 KO animals, although the cellular changes are less severe. Despite the reduction in scotopic a-wave amplitudes, rhodopsin levels are similar in the adult mice, across all genotypes irrespective of exposure to hyperoxia. Conclusions: Using the mouse model of ROP, we show that loss of Dio2 exacerbates the effects of hyperoxia-induced retinal deficits that persist in the adults. Our data suggest that aberrant Dio2/TH signaling is an important factor in the pathophysiology of the visual dysfunction observed in the oxygen-induced retinopathy model of ROP.
MeSH term(s)	Animals ; Animals, Newborn ; Blotting, Western ; Disease Models, Animal ; Electroretinography ; Enzyme Activators ; Hyperoxia/pathology ; Immunohistochemistry ; Iodide Peroxidase/physiology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Oxygen/metabolism ; Photoreceptor Cells, Vertebrate/enzymology ; Photoreceptor Cells, Vertebrate/physiology ; Retinopathy of Prematurity/enzymology ; Retinopathy of Prematurity/physiopathology ; Rhodopsin/metabolism ; Thyroid Gland/enzymology ; Iodothyronine Deiodinase Type II
Chemical Substances	Enzyme Activators ; Rhodopsin (9009-81-8) ; Iodide Peroxidase (EC 1.11.1.8) ; Oxygen (S88TT14065)
Language	English
Publishing date	2021-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.61.13.36
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Article ; Online: Neuronal Bmal1 regulates retinal angiogenesis and neovascularization in mice.

Jidigam, Vijay K / Sawant, Onkar B / Fuller, Rebecca D / Wilcots, Kenya / Singh, Rupesh / Lang, Richard A / Rao, Sujata

Communications biology

2022 Volume 5, Issue 1, Page(s) 792

Abstract: Circadian clocks in the mammalian retina regulate a diverse range of retinal functions that allow the retina to adapt to the light-dark cycle. Emerging evidence suggests a link between the circadian clock and retinopathies though the causality has not ... ...

Abstract	Circadian clocks in the mammalian retina regulate a diverse range of retinal functions that allow the retina to adapt to the light-dark cycle. Emerging evidence suggests a link between the circadian clock and retinopathies though the causality has not been established. Here we report that clock genes are expressed in the mouse embryonic retina, and the embryonic retina requires light cues to maintain robust circadian expression of the core clock gene, Bmal1. Deletion of Bmal1 and Per2 from the retinal neurons results in retinal angiogenic defects similar to when animals are maintained under constant light conditions. Using two different models to assess pathological neovascularization, we show that neuronal Bmal1 deletion reduces neovascularization with reduced vascular leakage, suggesting that a dysregulated circadian clock primarily drives neovascularization. Chromatin immunoprecipitation sequencing analysis suggests that semaphorin signaling is the dominant pathway regulated by Bmal1. Our data indicate that therapeutic silencing of the retinal clock could be a common approach for the treatment of certain retinopathies like diabetic retinopathy and retinopathy of prematurity.
MeSH term(s)	Animals ; Circadian Clocks/genetics ; Circadian Rhythm/genetics ; Mammals ; Mice ; Neovascularization, Pathologic/metabolism ; Photoperiod ; Retina/metabolism
Language	English
Publishing date	2022-08-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03774-2
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Article ; Online: Effect of Increasing Povidone-Iodine Exposure on Corneal Epithelium and Impact on Donor Rim Cultures.

Sawant, Onkar B / How, Stephanie / Hurlbert, Susan / Titus, Michael S / Vadakkepattath, Indu / Shen, Xiang / Djalilian, Ali R

Cornea

2022 Volume 41, Issue 12, Page(s) 1553–1558

Abstract: Purpose: The purpose of this study was to assess the effect of a second povidone-iodine (PVP-I) application at the time of donor tissue recovery on overall tissue quality and to analyze the rate of positive fungal and bacterial rim cultures before and ... ...

Abstract	Purpose: The purpose of this study was to assess the effect of a second povidone-iodine (PVP-I) application at the time of donor tissue recovery on overall tissue quality and to analyze the rate of positive fungal and bacterial rim cultures before and after implementing increased PVP-I exposure. Methods: The left cornea was recovered after a single application of PVP-I, while the right cornea was recovered after double PVP-I application in research-consented donors. The epithelial cell death rate was estimated using viability assay in corneal whole mounts under 10× objective (n = 5). Clinical characteristics of epithelium, stroma, and endothelium; positive rim culture rate; and incidences of infectious postoperative adverse reactions were compared for a period of 14 months before and after implementation of increased PVP-I protocol. Results: The average epithelial cell death rate was unaltered between single and double PVP-I exposure groups. We observed a modest 10% increase in the number of tissues with mild edema after implementation of increased PVP-I exposure. Nonetheless, the percentage of tissues with moderate or severe edema was unaltered. The average positive rim culture rate decreased from 1.17% to 0.88% (P = 0.075) after implementation of the double PVP-I soak procedure. There has been only one report of infectious postoperative adverse reactions since this procedure change. By contrast, there were 5 reports for a period of 14 months before implementation of this protocol. Conclusions: These results indicate that new donor preparation methods with an additional 5 minutes of PVP-I exposure do not affect tissue quality, reduce positive rim cultures, and lead to lower incidence of postoperative infection.
MeSH term(s)	Humans ; Povidone-Iodine ; Epithelium, Corneal ; Povidone ; Cornea/microbiology ; Edema
Chemical Substances	Povidone-Iodine (85H0HZU99M) ; Povidone (FZ989GH94E)
Language	English
Publishing date	2022-08-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	604826-2
ISSN	1536-4798 ; 0277-3740
ISSN (online)	1536-4798
ISSN	0277-3740
DOI	10.1097/ICO.0000000000003057
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